As a convention used herein, a nerve will be defined as a collection of individual nerve fibers (i.e., axons) of individual nerve cells (neurons) that together form an integrated pathway within the nervous system. Subsets of the individual nerve fibers are each bundled into one of a plurality of fascicles that together form the nerve. Action potentials can occur in the axon portion of individual nerve cells. A series of individual nerve fibers that together form an integrated signal pathway starting at a sensory-receptor nerve ending and extending to the brain will be referred to as a sensory-nerve pathway, a series of individual nerve fibers that together form an integrated signal pathway starting at the brain and extending to a muscle cell will be referred to as a motor-nerve pathway. Within each fascicle of a nerve, there will typically be a plurality of sensory-nerve pathways and a plurality of motor-nerve pathways, wherein the number of sensory-nerve pathways will typically be about fifteen times as many as the number of motor-nerve pathways. As well, a series of individual nerve fibers may together form an integrated pathway starting at one of various internal organs and ending in the brain, with then other series of individual nerve fibers together forming an integrated pathway starting at the brain and extending to some internal end organ (such as the digestive tract, the heart, or blood vessels) as part of the autonomic nervous system; and a series of individual nerve fibers may together form an integrated pathway within the brain referred to as a tract. As used herein, a nerve bundle or fascicle refers to a collection of nerve fibers that subserve a like function (e.g., a fascicle may support a plurality of different motor-nerve pathways and thus motor-control signals needed for the muscles for a hand grasp, for example; similarly the same and/or a nearby fascicle may support a plurality of corresponding sensory-nerve pathways and thus sensory signals that provide the brain with feedback for the hand grasp).
FIG. 1A is a schematic diagram 101 of a nerve (adapted from www.mayoclinic.org/peripheral-nerve-tumors-benign/diagnosis.html). A nerve 11 contains fascicles (bundles) 12 of individual nerve fibers 13 of neurons. FIG. 1B is a schematic diagram 102 of the structure of a spinal nerve 11 that includes its surrounding epineurium 14, which includes connective tissue and blood vessels 15, one or more fascicles (fasciculus) 12, each of which is surrounded by perineurium 17. Within a fascicle 12 is a plurality of axons 13 each having a myelin sheath surrounded by endoneurium tissue 18 (credit to internet sources: en.wikipedia.org/wiki/Nerve_fascicle and trc.ucdavis.edu/mjguinan/apc100/modules/nervous/pns/nervel/nervel.html).
Typically a nerve action potential (NAP) or compound nerve action potential (CNAP), which is a summated potential of the action potentials in all the axons in a nerve, as a signal travels down a nerve, is sensed using an electrical sensor probe that detects the waveform of a voltage associated with the NAP. Accordingly, traditional methods used electrical stimulation to trigger a NAP signal in a nerve. One disadvantage of using electrical stimulation is that the electrical signal applied to stimulate one nerve fiber will generally stimulate a plurality of surrounding nerve fibers (even nerve fibers in other fascicles than the fascicle containing the nerve of interest) to also trigger NAP signals in those other nerve fibers: Present neuromodulation technology is based on the generation of electric fields around the neuron. The spatial differential voltage along the axons, commonly referred to as the driving function, results in a depolarization of the neural membrane. This depolarization results in action-potential generation, which is then transmitted to target organ where it produces a characteristic effect. The electric field is significantly influenced by the electrical impedance of the tissues.
Extraneural electrodes, such as the Flat Interface Nerve Electrode (FINE), have demonstrated fascicular selectivity (to within about 400 μm (400 microns)). The perineurium, which surrounds a plurality of nerve axons and defines the individual fascicle, typically has a high impedance. This causes the voltage distribution to be fairly uniform within at least a portion of a fascicle (while also being electrically isolated from neighboring fascicles), hence limiting the possibility of sub-fascicular selectivity when using electrical stimulation. While the spatial selectivity of these extraneural electrodes (such as the FINE) has been successfully shown to produce functional neural stimulation in clinical applications, neuromodulation applications such as hand-grasp, sensory-stimulation applications for artificial prostheses, and control of autonomic functions such as cardiac rate via Vagus-nerve stimulation, require, in some cases, selection of at most one fascicle and even greater sub-fascicular spatial selectivity (i.e., selection of a single axon or just a few axons but not all the axons in the single fascicle) than is typically possible using electrical stimulation alone, such that separate signals are delivered to different axons within one fascicle.
Prior Innovations To Increase Selectivity With Electrical Stimulation:
A number of innovative electrode designs have advanced spatial selectivity for stimulation of nerve fascicles. The spiral electrode, introduced in 1988 (Naples, G. G., J. T. Mortimer, et al. (1988), “A spiral nerve cuff electrode for peripheral nerve stimulation,” IEEE Trans Biomed Eng 35(11): 905-16), has been shown in animal models to cause negligible changes in nerve morphology (Grill, W. M. and J. T. Mortimer (1998), “Stability of the input-output properties of chronically implanted multiple contact nerve cuff stimulating electrodes,” IEEE Trans. Rehabil. Eng. 6(4): 364-73; Grill, W. M. and J. T. Mortimer (2000), “Neural and connective tissue response to long-term implantation of multiple contact nerve cuff electrodes,” J Biomed Mater Res 50(2): 215-26) and was capable of selective stimulation (Sweeney, J. D., D. A. Ksienski, et al. (1990), “A nerve cuff technique for selective excitation of peripheral nerve trunk regions,” IEEE Trans Biomed Eng 37(7): 706-15; Sweeney, J. D., N. R. Crawford, et al. (1995), “Neuromuscular stimulation selectivity of multiple-contact nerve cuff electrode arrays,” Med. Biol. Eng. Comput. 33(3 Spec. No.): 418-25; Tarler, M. D. and J. T. Mortimer (2003), “Comparison of joint torque evoked with monopolar and tripolar-cuff electrodes,” IEEE Trans Neural Syst Rehabil Eng 11(3): 227-35). Twenty-one spiral electrodes have been implanted in five human subjects for periods between three months and three years without any observable loss of neural function that would be indicative of chronic damage. These electrodes have demonstrated moderate selectivity sufficient for neuromodulation in the upper and lower extremities. More refined applications require greater selectivity than currently achieved with the spiral electrode.
The Flat Interface Nerve Electrode (FINE), introduced in 2002 (Tyler, D. J. and D. M. Durand (2002), “Functionally selective peripheral nerve stimulation with a flat interface nerve electrode,” IEEE Trans Neural Syst Rehabil Eng 10(4): 294-303; also described in U.S. Pat. No. 6,456,866 issued to Tyler et al., discussed below), has been shown in animal models to attain a high level of fascicular stimulation and recording selectivity with negligible changes in nerve morphology (Tyler and Durand 2002 ibid.; Leventhal, D. K. and D. M. Durand (2004), “Chronic measurement of the stimulation selectivity of the flat interface nerve electrode,” IEEE Trans Biomed Eng 51(9): 1649-58; Tyler, D. J. and D. M. Durand (2003), “Chronic response of the rat sciatic nerve to the flat interface nerve electrode,” Ann Biomed Eng 31(6): 633-42; Yoo, P. B. and D. M. Durand (2005), “Selective recording of the canine hypoglossal nerve using a multicontact flat interface nerve electrode,” IEEE Trans Biomed Eng 52(8): 1461-9). Studies involving computational modeling have shown that the FINE electrode can selectively activate individual muscles within the femoral nerve stimulation (Schiefer, M. A., R. J. Triolo, et al. (2008), “A Model of Selective Activation of the Femoral Nerve with a Flat Interface Nerve Electrode for a Lower Extremity Neuroprosthesis,” IEEE Trans Neural Syst Rehabil Eng). The femoral nerve is composed of up to forty-three (43) fascicles in the dog or cat model, with several fascicles innervating each muscle. Electrical stimulation with the spiral and FINE electrode designs can be effective, but these electrode designs are limited in their ability to stimulate each of the forty-three (43) fascicles individually. Anatomic studies of the human upper extremity nerves show that these nerves have a large number of fascicles. Higher-precision spatial selectivity of individual nerve fascicles would enable more refined function to neuromodulation therapies, many of which still have ample opportunity for improved control of function.
To further increase fascicle and subfascicular selectivity, intrafascicular electrodes place stimulation electrodes within the individual nerve fascicles. Intraneural electrode arrays, such as the Utah Slanted Electrode Array (USEA) (see Branner, A. and R. A. Normann (2000), “A multielectrode array for intrafascicular recording and stimulation in sciatic nerve of cats,” Brain Res Bull 51(4): 293-306) and polymer longitudinal intrafascicular electrode (polyLIFE) (see Malmstrom, J. A., T. G. McNaughton, et al. (1998), “Recording properties and biocompatibility of chronically implanted polymer-based intrafascicular electrodes,” Ann Biomed Eng 26(6): 1055-64), penetrate through the perineurium to place contacts within the fascicles, in direct contact with axons. This has been demonstrated to be effective for selective stimulation, although there is evidence that this approach may cause damage to the nerve. Violation of the perineurium typically compromises the blood-nerve-barrier and other protective mechanisms of the perineurium. Owing to the simplicity and proven chronic experience of the circumneural approaches, an alternative method of stimulation that can improve the fascicular and subfascicular selectivity beyond the FINE would be a significant alternative to intrafascicular stimulation.
An emerging technology that significantly increases the spatial precision of nerve stimulation uses pulsed infrared light to reliably elicit neural action potentials in a non-contact manner (Wells, J. D., Kao, C., Jansen, E. D., Konrad, P., Mahadevan-Jansen, A., “Application of Infrared Light for in vivo Neural Stimulation,” Journal of Biomedical Optics, 2005; Wells, J. D., Kao, C., Mariappan, K., Albea, J., Jansen, E. D., Konrad, P., Mahadevan-Jansen, A., “Optical Stimulation of Neural Tissue in vivo,” Optics Letters, 2005. 30(5): p. 504-507, (collectively hereinafter “Wells et al. 2005”)). Infrared nerve stimulation (IRNS) was a result of an amalgamation of the fields of biomedical optics and neuroscience at Vanderbilt University. A systematic wavelength study using Vanderbilt University's tunable free-electron laser (2-10 μm) revealed that while most infrared wavelengths are capable of IRNS, 2.1 μm and 4 μm demonstrate the highest safety ratio for stimulation (safety ratio=laser radiant exposure required for thermal damage/laser radiant exposure required for stimulation resulting in a visible muscle twitch when stimulating the rat sciatic nerve). It was shown that IRNS using optimized laser parameters has a set of fundamental advantages over electrical stimulation that include high spatial selectivity, the ability to generate action potentials free of electrical stimulus artifact, non-contact stimulus delivery (even through bone), and MRI compatibility (Wells et al. 2005). These benefits make IRNS particularly attractive for clinical applications requiring precise, localized stimulation, such as use with diagnostic tools, neuroprostheses, and neurocognitive therapeutic devices.
Small, spatially localized neuronal populations have been stimulated with laser energy, which differs from the larger neuron populations that are stimulated by contemporary neural interfaces that use electrical current (Wells et al. 2005; Wells, J. D., Kao, Konrad, P., Mahadevan-Jansen, A., and Jansen, E. D. (2006), “Biophysical mechanisms responsible for pulsed low-level laser excitation of neural tissue,” Proc. SPIE 6084, 60840X (2006), DOI:10.1117/12.655239 (hereinafter “Wells et al. 2006”). Although important advances in spatial selectivity have been made in electrical stimulation (described above), the precision of electrical-stimulation techniques is fundamentally limited by the fact that electrical current spreads in a conductive medium (e.g., within a fascicle, since the tissue providing primary electrical insulation to prevent loss is the perineurium that surrounds the fascicle at its perimeter). A laser, on the other hand, offers a spatially restricted distribution of light that is predictable by the diffraction-limited spot size in the lateral direction, and a combination of the laser wavelength and the optical properties of the target tissue in the axial direction. This can have profound implications when applied to neuroprostheses. FIG. 2A and FIG. 2B illustrate the capability of optical stimulation to selectively activate specific fascicles within the main rat sciatic nerve to target specific muscle groups such as the gastrocnemius, while yielding no response from adjacent fibers that innervate the biceps femoris. Selective recruitment of nerve fibers is indicated by comparing the relative magnitudes of nerve and muscle potentials (FIG. 2A and FIG. 2B) elicited from optical and electrical stimulation. (Specifically, FIG. 2A and FIG. 2B show spatial targeting of IRNS. FIG. 2A shows threshold compound muscle action potential (CMAP) response from electrical stimulation of the main branch of the sciatic nerve proximal to the first branch point with 1.02 A/cm2. FIG. 2B shows corresponding results from threshold optical stimulation (0.4 J/cm2) of specific target nerve fibers that innervate the gastrocnemius, with no response from adjacent nerve fibers (quiet biceps femoris). The distance from the stimulation spot to recording electrodes was held constant for trials involving each modality (optical IRNS, electrical, or both) (as shown in these graphs, these signals were amplified with a gain=1000).) Results from these studies demonstrate subfascicular selectivity using infrared nerve stimulation (IRNS), thus providing motivation for applying this technique to neuroprostheses with the vision of greater selectivity and improved clinical outcomes in restoration of function.
Thus, recently, very specific optical-stimulation waveforms and wavelengths have been used to stimulate a nerve to trigger a NAP signal. Delivering such optical energy using optical fibers has the advantages of the very small structures of the optical fiber and the very small target areas to which the optical signal can be confined, which provides a medical practitioner the ability to stimulate one or only a few nerve fascicles within a nerve bundle without triggering NAPs in neighboring fascicles to which the medical practitioner does not wish to deliver triggering stimulation. Typically, a relatively high fluence of optical energy is required to trigger a NAP. In some embodiments, the present invention provides ability to stimulate spots that are much smaller than the fascicle and thus trigger NAPs on a subfascicular basis.
While research data suggest that infrared-nerve-stimulation (IRNS) technology has distinct advantages over other standard stimulation methods, there are a number of engineering challenges and obstacles that must be overcome before this technology matures to the point of clinical utility. A comprehensive set of survival studies to identify upper limits for safe laser intensities in the mammalian peripheral nerve have been undertaken. A low-frequency, short-duration stimulation protocol (2 pulses per second, 20 pulses) was applied to 50 nerves using a broad range of radiant exposures above stimulation threshold (0.4-1.4 J/cm2) with the research-grade Capella R-1850 infrared nerve stimulator (available from Lockheed Martin Aculight Corporation, 22121 20th Avenue S.E., Bothell, Wash. 98021), which provides improved nerve selectivity, no electrical artifact, and non-contact operation. Upper limits for radiant exposure to stimulate the rat sciatic nerve without thermal injury were evaluated using histology both 3-5 days (n=34) and 14 days (n=16) following stimulation, for assessment of any delayed neuropathology (such as Wallerian degeneration) in the stimulated nerves. An expert pathologist specializing in laser-tissue interactions reported any sign of epineurial or axonal damage as a 1, while if there were no detected signs of damage, this was reported as a 0 (zero). Statistical analyses (obtained using a software program (Probit v2.1.2, Litton TASC, San Antonio, Tex., 1998) for analyzing yes/no data on a log scale was applied to the data collected from survival experiments. Results from histological analysis (yes=damage, no=no damage) were input into the software program such that the output yielded the probability of damage as a function of laser radiant exposure. The 50% probability of damage was also determined in these computations) are summarized in graph 300 in FIG. 3, where the probability of damage is graphed as a function of radiant exposure for 3-to-5-day, and two-week survival experiments. (Specifically, FIG. 3 shows probability of damage as a function of laser radiant exposure compared to the stimulation threshold. Results from statistical analysis show the probability of histological nerve damage versus the laser radiant exposure from data collected from 3-to-5-day survival studies (crosses, n=34) and 14-day survival studies (triangles, n=16). The results from studies to determine the range of threshold radiant exposures needed for stimulation are shown for comparison with 95% confidence intervals. This graph illustrates that a safe margin exists between the maximum laser radiant exposures required to stimulate and the minimum radiant exposures necessary for damage (P(damage)=0%). These results quantify the upper limits for brief, low-repetition-rate optical stimulation of the rat sciatic nerve.)
The stimulation threshold (e.g., in some embodiments, this is the level of stimulation that achieves a 0.5 probability for stimulation—a response occurring upon 50% of stimulation occasions) in the rat sciatic nerve was shown to be 0.41+/−0.07 J/cm2 over a large number of trials (n=32). The radiant exposure with a 0.5 probability of thermal damage (damage occurring on 50% of occasions after a 2-Hz-and-20-pulses protocol as described in the previous paragraph) is 0.90 J/cm2 in the 3-5-day survival studies and 0.95 J/cm2 from two-week survivors. In some experiments, a fluence of less than 0.70 J/cm2 resulted in no thermal damage. While these data suggest that a small, but clearly defined “safe zone” exists when using a low-frequency, short-duration stimulation protocol, the approximately two-times (˜2×) safety margin may need to be improved before clinical implementation of this technique. In contrast, the safety margin for damage to stimulation thresholds in electrical stimulation is greater than fifty times (50×) in most peripheral nerves.
Other experiments report the upper limit for safe laser-stimulation repetition rate occurs near five (5) pulses per second and that the maximum duration for constant low-repetition-rate stimulation (two (2) pulses per second) is about four (4) minutes with adequate tissue hydration (Wells et al. 2005). It should be pointed out that the scenario above is specific to stimulation of the rat sciatic nerve (a peripheral nerve) and eliciting a visible motor twitch in the down-stream muscles. In other work, stimulation thresholds that are nearly two orders of magnitude lower have been reported while stimulating the spiral ganglion cells in the gerbil cochlea (Izzo, Richter et al., “Laser Stimulation of the Auditory Nerve,” Lasers in Surgery and Medicine, Wiley-Liss, Inc, 2006; Izzo, Suh et al., “Selectivity of neural stimulation in the auditory system: an comparison of optic and electric stimuli,” Journal of Biomedical Optics, 12(2), 021008 (March/April 2007); Izzo, Walsh et al., “Optical Parameter Variability In Laser Stimulation: a study of pulse duration, repetition rate, and wavelength,” IEEE Trans. Biomed. Eng., 2007 June; 54(6 Pt 1):1108-14). In those experiments it was also shown that continuous stimulation at 300 Hz for up to six hours did not result in reduction in CNAP signals from the stimulated cells. Another experiment on gerbil nerves was reported by Teudt et al. who exposed the gerbil facial nerve to 250-microsecond pulses of 2.12-micron-wavelength radiation from a Ho:YAG laser via a 600-micron-diameter optical fiber at a repetition rate of 2 Hz with radiant exposures of between 0.71 J/cm2 and 1.77 J/cm2 to trigger compound muscle action potentials (CmAPs) (Teudt et al., “Optical Stimulation of the Facial Nerve: A New Monitoring Technique?”, The Laryngoscope VOL: 117(9); p. 1641-7/200′709/, Lippencott Williams and Wilkins, 2007). Histology by Teudt et al. 2007 revealed tissue damage at radiant exposures of 2.2 J/cm2, but no apparent damage at radiant exposures of 2.0 J/cm2.
Increases in nerve-tissue temperature during laser stimulation may result in nerve-tissue damage. FIGS. 4A-4D show graphs of steady-state maximum temperature increase in nerve tissue from Ho:YAG laser stimulation. (Graph 401 of FIG. 4A: Temperature rise from 0.45 J/cm2 radiant exposure pulses at 2-Hz stimulation frequency. Graph 402 of FIG. 4B: Temperature rise from 0.65 J/cm2 radiant exposures at 2-Hz stimulation frequency. Graph 403 of FIG. 4C: Temperature rise from 0.41 J/cm2 threshold radiant exposures at 5-Hz stimulation frequency. Graph 404 of FIG. 4D: Temperature rise from 0.63 J/cm2 threshold radiant exposures at 5-Hz stimulation frequency.) The resultant heat load in tissue (measured via IR thermography) during low-frequency stimulation (graph 401 of FIG. 4A) has adequate time to diffuse out of the irradiated zone via conduction and other heat-transfer mechanisms. However, as indicated in graph 403 of FIG. 4C and graph 404 of FIG. 4D showing higher-frequency stimulation, temperature superposition will begin to occur at repetition rates greater than about 4 to 5 Hz, as the tissue requires slightly greater than 200 msec (milliseconds) to return to baseline temperature, since the thermal diffusion-time constant is ˜90 msec under these conditions. At repetition rates greater than 5 Hz tissue-temperature changes will become additive with each ensuing laser pulse, and resulting tissue damage may begin to occur with prolonged constant stimulation. These data also indicate that amount of temperature rise and the time to reach a steady-state temperature are dependent on the radiant exposure level. At lower radiant exposures the rise in temperature is smaller and reaches a steady-state temperature in a shorter time. What is needed is a means to reduce the radiant exposure levels required for reliable IRNS, which would greatly reduce the heat load (thus reducing the potential for tissue damage) and significantly advance the implementation of IRNS technology in highly precise neurostimulation devices.
U.S. Pat. No. 7,225,028 issued to Della Santina et al. on May 29, 2007, and titled “Dual Cochlear/Vestibular Stimulator with Control Signals Derived from Motion and Speech Signals,” is incorporated herein by reference. Della Santina et al. describe a system for treating patients affected both by hearing loss and by balance disorders related to vestibular hypofunction and/or malfunction, which includes sensors of sound and head movement, processing circuitry, a power source, and an implantable electrical stimulator capable of stimulating areas of the cochlea and areas of the vestibular system.
U.S. Patent Application Publication No. US 2007/0261127 A1 filed Jul. 24, 2006 by Edward S. Boyden and Karl Deisseroth, titled “LIGHT-ACTIVATED CATION CHANNEL AND USES THEREOF”; U.S. Patent Application Publication No. US 2007/0054319 A1 filed Jul. 24, 2006 by Edward S. Boyden and Karl Deisseroth, titled “LIGHT-ACTIVATED CATION CHANNEL AND USES THEREOF”; and U.S. Patent Application Publication No. US 2007/0053996 A1 filed Jul. 24, 2006 by Edward S. Boyden and Karl Deisseroth, titled “LIGHT-ACTIVATED CATION CHANNEL AND USES THEREOF,” are all incorporated herein by reference. These describe compositions and methods for light-activated cation channel proteins and their uses within cell membranes and subcellular regions. They describe proteins, nucleic acids, vectors and methods for genetically targeted expression of light-activated cation channels to specific cells or defined cell populations. In particular the description provides millisecond-timescale temporal control of cation channels using moderate light intensities in cells, cell lines, transgenic animals, and humans. The optically generated electrical spikes in nerve cells and other excitable cells are useful for driving neuronal networks, drug screening, and therapy.
U.S. Pat. No. 6,456,866, which issued to Tyler et al. on Sep. 24, 2002, titled “Flat interface nerve electrode and a method for use,” is incorporated herein by reference. Tyler et al. describe a flat interface nerve electrode (FINE) and a method for its use. The electrode provides a plurality of conductive elements embedded in a non-conductive cuff structure, which acts to gently and non-evasively redefine the geometry of a nerve through the application of a force so as to apply pressure to a nerve in a defined range. The cuff has an opening, which is elongated relative to the diameter of the nerve to which it is applied. Preferably, the cuff is constructed from an elastic bio-compatible material having top and bottom beam members configured to define a nerve opening. The cuff is open at one side and has a connection at the other side which results in a spring force being applied through the surfaces of the nerve opening to the subject nerve. During implantation the open sides of the cuff are closed so as to capture the nerve in the cuff. As the nerve is reshaped, specific nerve axons become more easily addressed through the epineurium by the embedded conductive elements.
U.S. Pat. No. 6,748,275, which issued to Lattner et al. on Jun. 8, 2004, and titled “Vestibular Stimulation System and Method,” is incorporated herein by reference. Lattner et al. describe an apparatus and method in which the portions of the labyrinth associated with the labyrinthine sense and/or the nerves associated therewith are stimulated to perform at least one of the following functions: augment or control a patient's respiratory function, open the patient's airway, induce sleep, and/or counteract vertigo.
U.S. Pat. No. 7,004,645, which issued to Lemoff et al. on Feb. 28, 2006, and titled “VCSEL array configuration for a parallel WDM transmitter,” is incorporated herein by reference. Lemoff et al. describe VCSEL array configurations. WDM is wavelength-division multiplexing. Transmitters that use several wavelengths of VCSELs are built up out of multiple die (e.g., ones having two-dimensional single-wavelength monolithic VCSEL arrays) to avoid the difficulty of manufacturing monolithic arrays of VCSELs with different optical wavelengths. VCSEL configurations are laid out to insure that VCSELs of different wavelengths that destined for the same waveguide are close together.
U.S. Pat. No. 7,116,886, which issued to Colgan et al. on Oct. 3, 2006, and titled “Devices and methods for side-coupling optical fibers to optoelectronic components,” is incorporated herein by reference. Colgan et al. describe optical devices and methods for mounting optical fibers and for side-coupling light between optical fibers and VCSEL arrays using a modified silicon V-groove, or silicon V-groove array, wherein V-grooves, which are designed for precisely aligning/spacing optical fibers, are “recessed” below the surface of the silicon. Optical fibers can be recessed below the surface of the silicon substrate such that a precisely controlled portion of the cladding layer extending above the silicon surface can be removed (lapped). With the cladding layer removed, the separation between the fiber core(s) and optoelectronic device(s) can be reduced resulting in improved optical coupling when the optical fiber silicon array is connected to, e.g., a VCSEL array.
U.S. Pat. No. 7,031,363, which issued to Biard et al. on Apr. 18, 2006, and titled “Long wavelength VCSEL device processing,” is incorporated herein by reference. Biard et al. describe a process for making a laser structure such as a vertical-cavity surface-emitting laser (VCSEL). The VCSEL designs described include those applicable to the 1200 to 1800 nm wavelength range.
U.S. Pat. No. 6,546,291, which issued to Merfeld et al. on Apr. 8, 2003, titled “Balance Prosthesis,” is incorporated herein by reference. Merfeld et al. describe a wearable balance prosthesis that provides information indicative of a wearer's spatial orientation. The balance prosthesis includes a motion-sensing system to be worn by the wearer and a signal processor in communication with the motion-sensing system. The signal processor provides an orientation signal to an encoder. The encoder generates a feedback signal on the basis of the estimate of the spatial orientation provides that signal to a stimulator coupled to the wearer's nervous system.
U.S. Pat. No. 6,171,239, which issued to Humphrey on Jan. 9, 2001 titled “Systems, methods, and devices for controlling external devices by signals derived directly from the nervous system,” is incorporated herein by reference. Humphrey describes a system to control prostheses and other devices with signals received by sensors implanted directly in the brain or other parts of the nervous system of a subject/patient and transmitted to an external receiver. The system has sensors in the form of bundles of small, insulated, flexible wires, configured in a parallel or twisted array, which are used to receive multicellular signals from small clusters of neurons. A new “calibration/adaptation” system is developed, in which the neural signals are cross-correlated with the parameters of a set of standardized or model movements as the subject/patient attempts to emulate the model movements, and on the basis of the correlations the neural signals that are best suited for control of the corresponding movement or movement parameter of the external device are selected. Periodic use of this calibration system compensates for or adapts to uncontrolled changes in neural signal parameters over time, and therefore results in re-selection of the optimal neural channels for better device control. Artificial neural nets are used for mapping the selected neural signals onto appropriate movements or control parameters of the external device.
Effective, specific and precise stimulation of selected nerves remains a problem. Improved apparatus and methods are needed to diagnose and/or treat various problems in animals (including humans).